A mutation that allows cells to grow out of control could also provide a new way to target and destroy cancer cells. This potential Achilles’ heel comes from a mutation in a gene called PTEN, which is found in a wide range of cancers.

PTEN is one of many tumor suppressor genes that we have to prevent our cells from growing out of control. If the PTEN gene stops working because of a mutation, it can cause tumours to develop – indeed many tumors have a mutated form of PTEN. However when a door closes, a window opens: the PTEN mutation helps the tumor to grow, but it could also mark it out as a target.

Researchers from the Institute of Cancer Research, London, found that switching off another gene known as NLK (Nemo-like kinase) killed tumor cells that had the PTEN mutation. This makes NLK a good target for drug developers to create a new cancer treatment.

Initially, the researchers took samples of tumor cells with and without the mutation, and switched off genes for important proteins that are used for regulating lots of processes in the cell. To do this they used small interfering RNA (or siRNA) which interfere with the processes of specific genes. These siRNAs block the chain of events that allow a gene to produce a protein, effectively switching it off. By switching off 779 genes individually, they could look for ones where cells with the PTEN mutation died and cells without the mutation survived.

This is how the researchers discovered the powerful effect of switching off the NLK gene. They are not certain how this works but it appears to protect a protein called FOXO1 that can act as a backup tumor suppressor and cause the cancer cell to die. When PTEN is mutated, the FOXO1 protein becomes vulnerable to a process called phosphorylation, which means it is ejected from the cell nucleus and destroyed. NLK is one of the proteins that phosphorylates FOXO1 and so by switching off the NLK gene, FOXO1 is able to do its job.

Growing older is not the same as aging. Everyone grows older all the time, but we aren’t necessarily aging as we do so since, by definition, the aging process is one of deterioration.

But we can actually grow new brain connections and even create new neurons from stem cells as a result of our thoughts. If you want to keep your brain and body healthy, you can start by adapting our suggestions into your personal plan.

The Summer 2017 issue of Conscious Lifestyle Magazine features Ray & Terry’s recommendations for building a better brain. As a Ray & Terry’s subscriber, we are happy to share the full article with you (pdf).

Researchers at the University of Florida have developed a new gene therapy that shows promise in fighting multiple sclerosis (MS). Testing the technique in mice, the team found that the treatment was effective in preventing animals from developing the mouse equivalent of the disease, and almost completely reversed the symptoms in those that were already suffering from it.

Save for the occasional burning pain that accompanies a run, most people don’t pay much attention to the two-leafed organ puffing away in our chests.

But lungs are feats of engineering wonder: with over 40 types of cells embedded in a delicate but supple matrix, they continuously pump oxygen into the bloodstream over an area the size of a tennis field. Their exquisite tree-like structure optimizes gas exchange efficiency; unfortunately, it also makes engineering healthy replacement lungs a near-impossible task.

Rather than building lungs from scratch, scientists take a “replace and refresh approach”: they take a diseased lung, flush out its sickly, inflamed cells and reseed the empty matrix with healthy ones.

If evolution works by selecting for the most advantageous genes, it begs the question: why haven't we evolved immortality? According to a decades-old hypothesis, certain genes that promote reproductive success also promote aging later in life, and now a study from Johannes Gutenberg University has identified some of these genes. The team also found that switching off those genes dramatically extended the lifespan of worms.

Getting old and dying is a natural part of life, but that doesn't mean we aren't interested in slowing or stopping it.

omeday in the not-too-distant future, getting rid of those unwanted "love handles" may be as easy as applying skin patches to your lower abdomen. In experiments on obese mice, researchers from Columbia University Medical Center and the University of North Carolina have successfully used such patches to slim the creatures down.

There are already drugs that convert energy-storing white fat into energy-burning brown fat, while also raising the body's metabolism. These have to be taken orally or via injections, however, so they affect the whole body. This causes side effects such as stomach upset, bone fractures and (ironically) weight gain.

slowly but surely, Alzheimer’s researchers finally seem to be giving the pathogen hypothesis a good, hard look. Harvard’s Tanzi, one of the newer microbial theorists, has been a prominent figure in the Alzheimer’s field for decades. He contributed to the 1987 discovery of APP, the first Alzheimer’s disease gene. Recently, Tanzi and his colleagues showed that amyloid-β inhibits the in vitro growth of pathogenic bacteria, including Candida albicans, E. coli, and Staphylococcus aureus, suggesting the Alzheimer’s-linked peptide was acting as an antimicrobial.9 Tanzi’s working hypothesis is that microbes trigger an innate immune response, in which amyloid-β plays a key role. The peptide surrounds the site of infection to shield healthy tissue from the invaders. Too much clumping, however, can cause problems of its own—the very processes by which plaques trigger neuronal death

A groundbreaking 2006 study found that fibroblasts – cells found in the skin and connective tissue – could be reverted back into stem cells by introducing four transcription factor genes, Oct4, Sox2, Klf4 and c-Myc (OSKM), into the nucleus of the cell. While this technique has been a useful way to create induced pluripotent stem cells (IPSCs) for a variety of medical purposes, it still has its risks. There's a chance the affected cells can turn cancerous for one, but even if they don't, their properties aren't always consistent.

"If you talk to cancer patients after surgery, one of the first things many will say is 'I hope the surgeon got all the cancer out,'" says Livia Schiavinato Eberlin, an assistant professor of chemistry at UT Austin who led the team. "It's just heartbreaking when that's not the case. But our technology could vastly improve the odds that surgeons really do remove every last trace of cancer during surgery."

Telling cancerous tissue apart from healthy tissue is key during surgery, and not just to ensure that all the tumor is removed. Taking too much healthy tissue can also be dangerous, raising the prospect of damage to muscle and nerve function, along with other painful side effects.

UCLA biologists have developed an intervention that serves as a cellular time machine — turning back the clock on a key component of aging.

In a study on middle-aged fruit flies, the researchers substantially improved the animals’ health while significantly slowing their aging. They believe the technique could eventually lead to a way to delay the onset of Parkinson’s disease, Alzheimer’s disease, cancer, stroke, cardiovascular disease and other age-related diseases in humans.

Staphylococcus bacteria from people’s noses produce amino acids that curb secretions of antimicrobial proteins in the sinus, according to a report published yesterday (September 5) in Science Signaling. The amino acids activate sweet taste receptors present on sinus cells, suggesting that pharmaceutical inhibition of these receptors may have the potential to treat sinus infections.

“This work expands upon a direction of research involving taste receptors and identifies mechanisms by which Staphylococcus bacteria modulate host immunity via interactions with these receptors,” says Martin Desrosiers of the University of Montreal who was not involved with the project. “It also helps explain how bacteria can contribute to the development and persistence of chronic rhinosinusitis,” he adds.

Eating a diet high in fat and low in carbohydrates keeps mice living longer, healthier lives, according to two separate studies published in Cell Metabolism today (September 5).

One of the studies, conducted by researchers at the University of California, San Francisco, and the Buck Institute for Research on Aging in California, cycled mice on and off a ketogenic diet, which forces the body to produce fatty acids called ketone bodies to fuel metabolism through the severe limiting of carbohydrates. Those mice, which were given non-ketogenic diets one week and ketogenic diets the next, avoided obesity and memory decline and displayed reductions in midlife mortality, compared to mice on a control diet.

Some of the workhorses that keep the immune system in check are tiny proteins on the surface of cells encoded by a set of guardian genes — human leukocyte antigen (HLA) in humans and major histocompatibility complexes (MHC) in mice. Scientists have long known that certain common variants of the HLA/MHC genes protect against a range of autoimmune diseases, notably Type 1 diabetes.

Yet how these genes and the tiny cell proteins they regulate yield their immune-modulating effects has remained shrouded in mystery. Now, a study in mice led by scientists at Harvard Medical School reveals that at least one of these genes has a protective influence that is powerfully shaped by the trillions of intestinal bacteria collectively known as the gut microbiota.

Scientists have known for some time that ethanol can kill cancer cells, but several limitations held it back from becoming a broadly used treatment. A team at Duke University has recently developed a new type of ethanol solution that can be injected directly into a variety of tumors to potentially offer a new, safe, and cheap form of cancer treatment.

Ethanol ablation is a form of cancer therapy where ethanol is injected directly into a tumor.

A 35-year-old man who had been in a vegetative state for 15 years after a car accident has shown signs of consciousness after neurosurgeons in France implanted a vagus nerve stimulator into his chest — challenging the general belief that disorders of consciousness that persist for longer than 12 months are irreversible.

In a 2007 Weill Cornell Medical College study reported in Nature, neurologists found temporary improvements in patients in a state of minimal consciousness while being treated with bilateral deep brain electrical stimulation (DBS) of the central thalamus. Aiming instead to achieve permanent results, the French researchers proposed use of vagus nerve stimulation* (VNS) to activate the thalamo-cortical network, based on the “hypothesis that vagus nerve stimulation functionally reorganizes the thalamo-cortical network.”

The classic image of a robot is one clad in a rigid metal shell, but that might not be practical in situations where man and machine will need to work together. The emerging field of soft robotics is helping to make that collaboration safer, but recreating muscle is no easy task. Now, mechanical engineers from Columbia University have developed a synthetic soft muscle that's said to be much more simple to make and run than others, and is three times stronger than the real thing.

One day in 2006, while a postdoc in the Rockefeller University laboratory of Nathaniel Heintz, I had an unexpected eye-opener. Heintz showed me some electron microscopy images of Purkinje neuron nuclei in the murine cerebellum. They stunned me—the heterochromatin localization in the nucleus was different from anything I’d ever seen before. Rather than the dispersed, irregular patches with enrichment near the nuclear membrane typical of many cells, nearly all the heterochromatin was in the center of the nucleus, adhered to the single large nucleolus. Not only did heterochromatin organization look different, the volume of it in Purkinje neurons seemed much lower, too. Because links between DNA methylation and heterochromatin proteins were suggested in the literature, we thought that DNA methylation might be depleted in Purkinje neurons.

Many great scientific discoveries have arisen out of laboratory accidents, from the mistake that led to penicillin, to revelations of LSD's psychedelic properties after Albert Hoffman unexpectedly absorbed a dose through his fingertips in 1943. The latest serendipitous discovery comes from a cross-contamination accident that has revealed how a certain bacteria can stifle the efficacy of cancer drugs.

Caltech researchers have developed a “Fantastic Voyage” style prototype microchip that could one day be used in “smart pills” to diagnose and treat diseases when inserted into the human body.

Called ATOMS (addressable transmitters operated as magnetic spins), the microchips could one day monitor a patient’s gastrointestinal tract, blood, or brain, measuring factors that indicate a patient’s health — such as pH, temperature, pressure, and sugar concentrations — with sub-millimeter localization and relay that information to doctors. Or the devices could even be instructed to release drugs at precise locations.

We could be in for a Fantastic Voyage-style future where tiny medical devices swim through our bodies to deliver drugs or diagnose diseases, but keeping track of all those little explorers can be tricky. A new invention out of Caltech might help make that easier. It's a chip loaded with sensors that can ping its location in the body, thanks to MRI-inspired technology.

It can be hard to check the inner goings-on of a patient's body without being too invasive, but "smart pills" could provide an easy-to-swallow alternative. So far, these diagnostic devices include the likes of a sensor to measure gas concentrations in the intestine, and a tiny camera to snap images where colonoscopies can't reach. The new Caltech device could eventually be part of these systems, allowing doctors to monitor the pill's progress through the patient.

Biologists often concern themselves with preserving cells. However, it is also advantageous to learn how to kill them, without having their contents exploding into neighboring tissue. That's exactly what bioengineers have done by linking a "suicide" enzyme with a light-sensitive molecule.

Early intervention is key when trying to combat dementia-related disease. A new long-term study by researchers at Michigan State University has provided evidence that a straightforward scratch-and-sniff test could effectively direct doctors towards those with a high risk of developing Parkinson's years before the disease exhibits notable symptoms.

Strong research from a variety of sources has previously suggested that a decrease in a person's sense of smell could be linked to the very early stages of Alzheimer's disease. This new study, conducted over 10 years, has focused on the development of Parkinson's disease in a multiracial cohort of subjects.

In late 2011, Drexel University dermatology professor Herbert Allen was astounded to read a new research paper documenting the presence of long, corkscrew-shape bacteria called spirochetes in postmortem brains of patients with Alzheimer’s disease.1 Combing data from published reports, the International Alzheimer Research Center’s Judith Miklossy and colleagues had found evidence of spirochetes in 451 of 495 Alzheimer’s brains. In 25 percent of cases, researchers had identified the spirochete as Borrelia burgdorferi, a causative agent of Lyme disease. Control brains did not contain the spirochetes.

The study made Allen think back to 40 years earlier, when he was an intern at Johns Hopkins University and had treated a patient diagnosed with neurosyphilis, a neurological syndrome that included dementia and resulted from the invasion of the syphilis spirochete into the brain. “The parallel between Lyme disease and syphilis had me intrigued,” he says.

For well over half a century, scientists have been working to harness the cell-destroying power of viruses in the battle against cancer. The latest addition to this arsenal comes from an unlikely source, the relatively new Zika virus, which could offer a new way to fight deadly brain cancers.

A virus that is found to target and kill cancer cells is known as an oncolytic virus, and over the years scientists have worked to engineer a number of different viral strains with this ability. The biggest challenge faced by scientists in the field has been finding ways to manipulate the viruses into a state that makes them safe to use in a clinical environment, but retains their effectiveness as a cancer-killing agent.

Are carbs the new fat? For much of the second half of the 20th century, doctors constantly suggested we avoid high-fat foods, but more recently a new target for our dietary scorn has emerged: carbohydrates. Two new companion studies are suggesting a ketogenic diet – high fat, low protein, and low carbohydrates – could enhance memory, improve physical strength and extend lifespan.

In 2015, scientists from Rice University revealed they had created light-driven nanosubmarines. These tiny molecular machines were activated by ultraviolet light and based on earlier work from Nobel laureate Bernard Feringa, whose ground-breaking research won the prize for chemistry in 2016. These single-molecule machines have now been shown to be able to target, and drill into, specific cancer cells, paving the way for a variety of highly targeted future nanomedicine treatments.

The FDA has just approved Kymriah, a new form of genetically modified T-cell immunotherapy for treating young patients with a type of blood and bone marrow cancer. This is the first gene therapy of its kind to be approved for use in the United States, but the treatment is not without controversy as it has the potential for severe side effects as well as an extraordinarily prohibitive price tag.

It's not hyperbolic to say that the development of CAR-T immunotherapy has been a revolution in cancer research over the past few years. The therapy involves harvesting a patient's T-cells and then genetically modifying them to hold potent molecules called chimeric antigen receptors (CARs). These CAR-T cells are then reintroduced into the patient and act as cancer hunters, targeting and killing specific tumor cells.

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